Also known as: ACTH(4-10) analogue · Met-Glu-His-Phe-Pro-Gly-Pro · Семакс
| Parameter | Value | Source |
|---|---|---|
| Elimination Half-Life (Intranasal) | ~minutes (estimated; proteolytic) | Animal study data; Miasoedov NF et al. 2008 |
| Tmax (Intranasal) | ~5–15 min (animal data) | Animal pharmacokinetic studies |
| Route(s) of Administration | Intranasal spray; SC injection (some protocols) | — |
| CNS Penetration (Intranasal) | Documented via olfactory route in animal models | Animal study data |
| Plasma Protein Binding | No published data | — |
| Full Clearance (5 half-lives) | ~60–90 min estimated | Inferred from heptapeptide proteolytic kinetics |
| Cognitive Effect Duration | ~4–8 hours (animal models) | Animal studies |
| Standard Dosing | 200–2,000 µg intranasal daily (Russian clinical practice) | Miasoedov NF et al. 2008 |
| Data Quality | Animal Study + limited Russian human trials — No English-language human PK study published (as of May 2026) | |
Semax (ACTH 4-10 analogue; sequence Met-Glu-His-Phe-Pro-Gly-Pro) has a plasma half-life estimated at minutes after intranasal administration, based on animal pharmacokinetic data and the known rapid proteolytic degradation of heptapeptides in nasal mucosal tissue and plasma.[1] No formal human pharmacokinetic study has been published in PubMed-indexed English-language peer-reviewed literature as of May 2026. Available data is from Russian-language clinical literature and animal studies.
Semax was developed at the Institute of Molecular Genetics, Russian Academy of Sciences, and approved in Russia in 1996. It is used clinically in Russia for stroke rehabilitation, cognitive impairment, optic nerve disease, and as a general nootropic agent. It is not approved by the FDA in the United States.
The ~minutes half-life estimate is inferred from: (1) animal pharmacokinetic studies in rodents showing rapid plasma clearance of the heptapeptide after intranasal administration; (2) the known susceptibility of the Met-Glu-His-Phe-Pro-Gly-Pro sequence to nasal mucosal aminopeptidases and plasma proteases; and (3) structural analogy with ACTH(4-10), the parent sequence, which has rapid plasma turnover.[1][2] A formal two-compartment model or terminal half-life derived from human plasma concentration-time data does not exist in the published English-language literature.
Semax's ~minutes plasma half-life contrasts sharply with its reported cognitive effect duration of several hours in animal models and in Russian clinical use. This PK/PD dissociation is the defining feature of short-half-life nootropic peptides. Semax is proposed to act by upregulating brain-derived neurotrophic factor (BDNF), inhibiting enkephalin-degrading enzymes, and modulating serotonergic and dopaminergic neurotransmission — all mechanisms that produce lasting downstream effects independent of ongoing drug plasma levels.[2][3]
Based on the estimated minutes-range plasma half-life, Semax is expected to reach pharmacologically negligible plasma levels within approximately 60–90 minutes of intranasal dosing (5× estimated t½ of ~12–18 minutes). This is an inferred estimate, not a measured human value.
| Phase | Approximate Time | Plasma Status | Note |
|---|---|---|---|
| Tmax (peak plasma) | ~5–15 min post-dose | Peak | Animal data; intranasal absorption via olfactory route |
| 50% decline | ~10–20 min | 50% of Cmax | Estimated from heptapeptide proteolytic kinetics |
| Near-complete plasma clearance | ~60–90 min | ~3% of Cmax | Estimated; no published human measurement |
| Cognitive effect duration | ~4–8 hours (animal) | Plasma < detection | Effects outlast plasma presence via BDNF/neurotransmitter mechanisms |
The intranasal route is used for Semax because it (1) bypasses GI proteolysis that would destroy the heptapeptide, and (2) achieves partial direct CNS delivery via olfactory nerve pathways, similar to intranasal oxytocin and other neuropeptides. The ~minutes plasma half-life means repeated intranasal administration is needed to maintain any CNS signaling, though the downstream effects (BDNF upregulation, enzyme inhibition) outlast individual doses.[1]
Russian clinical protocols use 200–2,000 µg intranasal daily, often in the morning, for nootropic purposes, or twice daily in neurological rehabilitation contexts. These regimens are derived from Russian clinical trial data, not from formal PK-guided dosing studies.
| Compound | Class | Half-Life | Route | Primary Effect | Approval |
|---|---|---|---|---|---|
| Semax | ACTH(4-10) analogue | ~minutes (IN, estimated) | Intranasal | Nootropic / neuroprotective | Russia; not FDA |
| Selank | Tuftsin analogue | ~minutes (IN, estimated) | Intranasal | Anxiolytic / nootropic | Russia; not FDA |
| DSIP | Neuropeptide | ~40 min (IV) | IV / SC | Sleep regulation | Not approved |
| Route | Half-Life | Notes |
|---|---|---|
| Intranasal | ~minutes (estimated from animal data) | Standard approved route in Russia; CNS penetration via olfactory pathway documented in animal models |
| Subcutaneous | No published human PK data | Used in some research protocols; systemic absorption expected but not formally characterized |
| Intravenous | No published human PK data | Not a clinical route; not characterized |
| Oral | Not viable | Proteolytic degradation by GI enzymes; not bioavailable |
Semax is not included in any standard WADA or workplace drug test panel. It has no psychoactive abuse potential that would trigger standard panel inclusion, and it is not scheduled in the US.
No published forensic detection window study characterizing Semax urinary detection by LC-MS/MS or other specialized methods has been identified in PubMed-indexed literature. Given the estimated ~minutes plasma half-life, detectable plasma or urinary levels would be expected to be limited to approximately 1–2 hours after intranasal dosing using specialized methods, though this is inferred rather than measured.
Semax is a synthetic heptapeptide analogue of the adrenocorticotropic hormone (ACTH) fragment 4–10 (Met-Glu-His-Phe-Pro-Gly-Pro), modified for metabolic stability relative to the native ACTH fragment. The Pro-Gly-Pro C-terminal extension was added to improve resistance to aminopeptidase degradation and enhance CNS bioactivity, though this stability is relative — plasma clearance remains rapid compared to larger proteins.[2]
Proposed mechanisms in animal studies include: (1) upregulation of BDNF (brain-derived neurotrophic factor) and NGFI-A expression in hippocampus and frontal cortex; (2) inhibition of enkephalin-degrading enzymes (leucine aminopeptidase, prolyl endopeptidase), thereby elevating endogenous opioid tone; (3) modulation of serotonin and dopamine neurotransmitter systems; and (4) direct melanocortin receptor (MC4R) activity inherited from the ACTH(4-10) parent sequence.[3]
The proposed neuroprotective mechanism in stroke models involves reduced glutamate excitotoxicity and VEGF upregulation. These effects have been demonstrated in rodent models but formal human RCT data is limited to Russian-language clinical literature.
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